PLANT STRESS RESPONSE

STRESS

• Manifold unfavourable, but not necessarily immediately lethal conditions, occurring either permanently or sporadically in a locality

• Significant deviation from optimal conditions for life

• Elicit responses and changes at all functional levels of the organism

• May be first reversible, but may become permanent

STRESS

• Conditions that adversely affect growth, development, productivity

1.Abiotic (phy/che environment)2.Biotic (organisms)• Abiotic- water logging, drought, high or low

temperatures, excessive soil salinity, inadequate mineral nutrients, too much or too little light, ozone

RESISTANCE

• Depends on1.Species2.Genotype3.Age of plant4.Tissue identity5.Duration, severity, rate of stress

1. Alarm phase – stress reaction2. Restitution- repair3. Hardening4. Adjustment5. Adaptation- normalization6. (Exhaustion)- irreversible damage7. End phase

STRESS RESPONSE

• Race b/w effort to adapt and potentially lethal processes in protoplasm

• Triggered by stress or stress- induced injury (membrane integrity loss)

• Some- enable plant to acclimatize to stress

• Altered gene expression- changes in development, metabolism

• Initiated when plant recognizes stress at cellular level- proteins that sense abiotic stress

• Transmit information within individual cells and through out the plant

• increase in specific mRNA, enhanced translation, stabilization of proteins, alteration of protein activity

WATER DEFICIT

• Major a biotic stress• Induced by many environmental conditions:1.No rainfall- drought2.High salt conc.3.Low temp.4.Transient loss of turgor at midday• Rate of onset, duration, acclimatization-

influence the water stress response

Response to water deficit• ABA phytohormone• Induce expression of drought- inducible genes• Products- 2 groupsA.GROUP 11.Protective proteins2.Water channel proteins, membrane transporters3.Osmoregulator synthesizing enzymes4.Detoxifying enzymes (peroxidases, catalases)

B) GROUP 21.Transcription factors (DREB, MYC)2.Protein kinases (MAP kinases, CDP kinases)3.Proteinases (phospholipase)

• 4 independent pathways1)2 - ABA-dependent2)2 - ABA- independent• Cis acting elements- in promoter of all stress

inducible genes- ABA-responsive element (ABRE) dehydration responsive element (DREB)

COLD- STRESS • Plants produce a no. of proteins in response to cold

and freezing temp.• 54 cold inducible genes• 10% of drought induced genes- also induced by cold• Genes- contain a cis element repeat (CRT)- 5 bp seq.• Transcription factor- C repeat binding factor (CBF)-

Main controlling switch in monocots, dicots

Cold stress reactions

• Injury to cell membrane – chilling, freezing• Ratio of saturated to unsaturated fatty acids-

degree of tolerance, particularly in plastids• Non- acclimatized plants- killed or injured at -

100 C or below.• Freeze acclimatized trees- survive between -40

to -500C• Injury- by severe dehydration during freeze-

thaw cycles

• Temp below 00C , cellular water freeze.

• Cell shrinkage

• Expansion induced lysis

• SURVIVAL STRATEGIES: anti freeze proteins (AFP)- Declines rate of ice crystal growth- Lowers the efficiency of ice nucleation sites- Lowers temp. at which ice formsOsmoprotectants- osmolytes- quarternary amines, amino acids,

sugar alcohols- Balances the osmotic potential of externally

increased osmotic pressure

• Glycine betaine • Quaternary amine, soluble• CH3 gps- interact with hydrophobic and

hydrophilic molecules• Oxidation- choline (choline monooxygenase)> betaine aldehyde• Betaine aldehyde (betaine aldehyde dehydrogenase)>

glycine betaine

• Proline

• Sugar alcohols –mannitol

• Trehalose- non reducing disaccharide• Increased water retention and desiccation

tolerance

SALT STRESS

• Flow of water is reversed- imbalance• Accumulation of excess Na+, Cl- in cytosol• Stress tolerant plants- maintains internal

osmotic pressure

Sensing salt stress• Ion specific signals of salt stress• High Na+- increases Ca2+ conc. In cytoplasm- Key

component of Na+ signalling• SOS3 – Ca2+ binding protein• Activates protein kinase (SOS2)• Phosphorylates (activates) plasma membrane H+-Na+

antiporter (SOS1)• SOS1 mRNA- stabilized, accumulates

-

• Plant maintains high K+, low Na+ in cytosol• 3 tolerance mechanisms-1)Reducing Na+ entry to cells2)Na+ efflux from cell (K+-Na+)3)Active transport to vacuole (vacuolar H+-Na+

ATPase)

Na+ sequestration

• In vacuoles• By NHX1, NHX2 proteins of tonoplast

membrane• Decreases cytoplasmic Na+

Salt stress induced proteins

• Transcription of genes oncoding late embryogenesis abundant (LEA) proteins- activated

Antioxidant production

• Abiotic stress – drought, salt, chill- increases reactive O intermediates (ROI) in plants

• ROI- stress signal- due to altered metabolic functions of chloroplast, mitochondria

ROI SCAVENGINGAntioxidant system contains a battery of

enzymes that scavenge ROI- SOD, peroxidases, catalases, glutathione reductases

HEAT STRESS

• Decrease in synthesize of normal proteins• Transcription and translation of HSPs• When 5o C rise in optimum temp.• Conserved proteins• Act as chaperons, refolding• classes- based on mw• Hsp 100, Hsp 90, Hsp 70, Hsp60

FLOODING

-Decreases O2 availability of plant roots-ATP production is lowered -SURVIVAL STRATEGIES: production of enzymes

for sucrose, starch degradation, glycolysis, ethanol fermentation

-ethylene- long term acclimatization responses-stem elongation

BIOTIC STRESSES

INDUCED STRUCTURAL AND BIOCHEMICAL DEFENCES

• Plants receive signal molecules as soon as pathogen contact

• Elicitors of recognition• Host receptors – on plasma membrane or

cytoplasm• Bichemical reactions, structural changes – to

fend off pathogen, toxins

Signal transduction

• Transmission of alarm signal to host defense providers

• To host proteins, nucleur genes- activated- products that inhibit pathogen

• Signals to adjacent cells, usually systematically• Intracellular signal transducers- protein

kinases, Ca2+ ,phosphorylases, phospholipases, ATPases, H2O2,ethylene.

• Systemic signal transduction, aquired resistance- by salicylic acid, oligogalacturonides from plant cell walls, jasmonic acid, systemin, fatty acids, ethylene

Induced structural defenses

• After pathogen has penetrated preformed defense structures- plant respond by one or more structures to prevent further pathogen invasion

• Defense structures: 1) cytoplasmic defense reaction 2) cell wall defense structures 3) histological dfense structures 4) necrotic/ hypersensitive defense reaction

Cytoplasmic defense reaction

• In response to weakly pathogenic and mycorrhizal fungi

• Induce chronic diseases / nearly symbiotic conditions

• Cytoplasm surrounds hyphal clump• Cytoplasm and nucleus enlarge• Dense granular cytoplasm • Mycelium disintegrates, invasion stops.

Cell wall defense structures• Morphological changes of cell wall• Limited effectiveness• a) parenchymatous cells’ walls swell, produces

amorphous, fibrillar material that surrounds, traps bacteria

• b) cell wall thickens by a cellulosic material infused with phenolics

• c) callose papillae laid of inner surface of cell wall (2-3 mins ) (fungi)

formation of lignituber around fungal hyphae

Histological defense structures• Formation of cork layers- fungi, bacteria, virus,

nematodes inhibits invasion beyond initial lesion prevents flow of nutrients• Abscission layers- fungi, bacteria, virus gap b/w 2 circular cell layers surrounding infection site• Tyloses- over growth of protoplasts of adjacent

parenchymatous cells- protrude into xylem vessels through piths

• Gums- around lesions intracellular spaces, within surr. cells.

ABSCISSION LAYER

TYLOSE FORMATION

Necrotic defense reaction

• Hypersensitive response• Brown resin-like granules in cytoplasm• Browning continues, cell dies• Invading hypha- degenerates• Bacterial infections- destruction of cell

membranes, desiccation, necrosis of tissue• Obligate parasites- fungi, bacteria, nematode,

viruses

INDUCED BIOCHEMICAL DEFENSES

HYPERSENSITIVE RESPONSE(HR)• Initiated by elicitor recognition• Rapid burst of oxidative reactions• ↑sed ion movement (H+, K+)• Loss of cellular compartmentalization• Crosslinking of phenolics with cell wall• Production of antimicrobials

HR

• due to plant R (resistance) gene • Pathogen produced elicitor- from its

Avirulence gene• Eg:- arv D gene of P. syringae- enzyme

involved in synthesis of syringolides (hypersensitive response in soya bean)

• Eg:- protein of tobacco R gene- protect against leaf spotting bacterium – in cytoplasm

• Eg:- protein of Cf9 R gene of tomato- against race 9 of leaf mould fungus- outside plasma membrane

ACTIVE O RADICALS, LIPOXYGENASES, CELL MEMBRANE DISRUPTION

• Pathogen attack, exposure to toxins, enzymes-permeability changes of plasma membrane

• Membrane ass. Disease response – 1. release of signal transduction molecules

systematically2.Release, accumulation of O radicals,

lipoxygenases3.Activation of phenol oxidases, oxidation of

phenolics

• O2-, H2O2, .OH released by multi subunit NADPH oxidase enzyme complex of plasma membrane

• Sec or mins• Hydroperoxidation of membrane

phospholipids, forming lipid hydroperoxides (toxic)

• Involved in HR induced response• Oxidises phenols to more toxcs quinones• Lipoxygenases oxidizes membranes as well

• Lipoxygenase generated hydroperoxides fom unsaturated fatty acids- lin, len

→converted to bio active molecules- jasmonic acid

role in wound and stress response

Antimicrobials

• Pathogenesis related proteins (PR)- toxic to invading fungi

• Trace amounts normally, but high after pathogen attack (stress induced trancscription)

• Extremely acidic or basic – hence soluble, reactive

• PR1, chitinases, β 1,3-glucanases,proteinases, peroxidases, cystein rich proteins

Phytoalexins

• Antimicrobials produced by phytopathogens/ chemical/ mechanical injury

• inhibit fungi, also toxic to bacteria, nematodes• Chemical structure- quite similar• Eg;- isoflavonoids in legumes• Accumulates around healthy cells around

wounded cells• Phytoalexin elicitors- glucans, chitosan,

glycoproteins (constituents of fungal cell wall)

OTHER MECHANISMS

• SIMPLE PHENOLICS- chlorogenic acid, caffeic acid

• TOXIC PHENOLICS FROM NON-TOXIC PHENOL GLYCOSIDES (sugar+ phenolic)- microbial glycosidases

• DETOXIFICATION OF PATHOGEN TOXINS- Eg:-fungal HC toxin (Cochliobolus carbonum),Pyricularin (Magnoporthe grisea)